Calcium in the Ischaemic Myocardium

  • Winifred G. Nayler
Part of the NATO Advanced Science Institutes Series book series (NSSA, volume 62)


Injured cardiac myocytes accumulate Ca2+. It does not seem to matter whether the injury is due to reperfusion after prolonged periods of normothermic ischaemia (Shen and Jennings 1972a,b., Nayler 1981), sustained hypoxia (Nayler et al, 1979), a naturally occurring cardiomyopathy, or the reintroduction of Ca2+ after only a few minute’s of Ca2+-free perfusion (Nayler and Grinwald 1982), the end result is the same — that is, the cells become overloaded with Ca2+. The primary aim of this paper is to establish why injured myocytes accumulate Ca2+, particularly during reperfusion after a prolonged period of ischaemia, and then to define the route by which this Ca2+ enters.


Sarcoplasmic Reticulum High Energy Phosphate Ischaemic Episode Slow Channel Myocardial Ischemic Injury 
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Copyright information

© Plenum Press, New York 1983

Authors and Affiliations

  • Winifred G. Nayler
    • 1
  1. 1.Department of Medicine, Austin HospitalUniversity of MelbourneHeidelbergAustralia

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